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Consumption of greater amounts of protein are not effective in further stimulating MPS and instead result in oxidation of the excess amino acids .
The stimulatory effect of acute hyperaminoacidemia on MPS is short-lived, lasting ~90 min [11, 12] after which MPS returns to baseline even in the presence of sustained elevations in plasma amino acid concentration [11, 12]; a phenomenon recently termed the “muscle-full effect” .
The extent of the aging-induced decline in muscle mass and strength has been linked to a greater risk of physical impairment, reduced quality of life and death [1, 2] with healthcare costs associated with sarcopenia estimated to cost .5 billion per year in the United States in 2000 .
As a result, development of low-cost therapeutic approaches to combat the deleterious effects of sarcopenia are vitally important to a U. population projected to become considerably older over the coming decades .
Muscle mass is determined by the balance of the rates of muscle protein synthesis (MPS) and breakdown (MPB) with skeletal muscle protein turnover a tightly controlled process in healthy adults, typically proceeding at a rate of ~1–2% per day. Although rates of MPS and MPB fluctuate throughout the day the majority of time is spent in the postabsorptive state where the rate of MPB is ~30–40% greater than MPS [5, 6].In the United States total omega-3 fatty acid intake is typically between 1.4 and 1.6 g per day [39–41] with the majority (~90%) consumed as α-linolenic acid (ALA; C18:3 models supporting a stimulatory effect of omega-3 fatty acids on MPS.For example, a greater anabolic response to mixed nutrient feeding was observed following consumption of a DHA-enriched diet for 34 days in growing pigs with no effect on fasting MPS .As a consequence of aging-induced dysregulation of MPS (and probably also MPB) muscle mass loss occurs at a rate of ~0.5–1.0% per year from the 5 setting when results are normalized to fiber size .This finding differs to in intact humans where the deterioration in muscle function occurs at ~2–3-fold greater rate than the loss of muscle mass (declines of ~2–3% vs. The reduction in muscle quality (i.e., strength per unit of muscle mass) with aging has been postulated to be occur due to changes in the muscle architecture , an increase in intermuscular fat infiltration [32–34], greater muscle fibrosis [35, 36], and reduced neuromuscular activation [37, 38].